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I read with great interest the case report in the December 2009 issue of JAOA—The Journal of the American Osteopathic Association by John M. Lavelle, DO, and Mark E. McKeigue, DO,1 regarding osteopathic manipulative treatment (OMT) of a patient with drop foot. Lavelle and McKeigue1 reported that a single 15-minute OMT session resolved their patient's symptoms. I have had extensive experience treating patients with OMT for nerve compression, particularly carpal tunnel syndrome, over 3 decades.2-5 Yet, I have never enjoyed the experience of seeing a patient get off the examination table with instantaneous recovery of three grades of muscle strength—from a grade of 1/5 to one of 4/5.

I commend the authors' recognition of the cause of nerve injury in the case they present (ie, a compressed common peroneal nerve caused by posterior fibular head dysfunction), as well as their knowledge and abilities to apply OMT at the fibular head to alleviate the nerve compression. However, although the authors properly describe the patho-anatomic condition of the patient, they do not address the pathophysiologic change that explains the remarkable and rapid resolution of muscle weakness in this case.1 It was obviously a case of motor conduction block, also known as neurapraxia.6 Neurapraxic lesions most commonly result from acute nerve compression, and “recovery is complete within days or weeks,” according to Oh.6

Oh6 also notes that it is important to recognize those cases that involve neurapraxia “because of the good prognostic implication” in such cases. A determination of neurapraxia can be obtained only with electrodiagnostic (EDX) testing, which is vital to rule out other causes of drop foot.7 These other causes commonly include L5 radiculopathy, lumbosacral plexopathy, motor neuron disease, and sciatic mononeuropathy.7

Wilbourn,8 who has written extensively on peroneal neuropathy, states, “The EMG [electromyographic] examination is a superb diagnostic study for the evaluation of foot-drop [ie, drop foot] in general and peroneal mononeuropathies in particular.” Wilbourn8 classifies the conduction block type of lesion as “Type 2.” This type of lesion is common, though it is not seen as often in the clinical setting as the “Type 1” pattern of mixed axon loss and conduction block.8 Wilbourn8 also notes that conduction block lesions have an “excellent prognosis” and rarely require surgical intervention.

Typically, conduction block lesions do not become apparent (via EDX testing) until 7 to 10 days after the nerve becomes compressed.8 Therefore, it appears that Lavelle and McKeigue1 made a reasonable decision to avoid EDX testing in the case of their patient, who first noticed symptoms the day before visiting the primary care office.

Many osteopathic physicians may believe that an immediate and rapid recovery as described by Lavelle and McKeigue1 is unlikely, and that the patient's “recovery” may instead suggest a type of pseudoparalysis, possibly induced by pain inhibition. Nevertheless, the literature supports such a recovery in the early phase of acute motor conduction block. In their classic 1944 study, Denny-Brown and Brenner,9 who applied external pressure to laboratory animals' nerves and measured the times to paralysis and recovery, noted the following:

Further, the time of recovery might be expected to vary in proportion to the latent period, for the more complete the ischemia the less rapid should be the recovery. No such relationship was observed. Recovery tended to either begin immediately or to be much delayed, without relation to the pressure employed or to the latent interval of conduction failure. Thus, after exposure to 56 cm of pressure, with failure of conduction in twenty-seven minutes, recovery in 1 experiment began immediately on release. In another experiment, after failure in twenty-five minutes, recovery began six minutes after release.

The case presented by Lavelle and McKeigue1 is extremely unusual. It is highly unlikely that the average osteopathic physician will see a patient arrive at his or her office 1 day after onset of a relatively benign neurapraxic lesion, and that the osteopathic physician will know how to apply OMT to resolve the patient's condition. An osteopathic physician may be more likely to encounter a patient who has been experiencing foot drop symptoms over an extended period—cases that would not be neurapraxia. I am concerned that the authors did not emphasize the importance in such cases of pursuing a definitive diagnostic workup and considering alternative or more aggressive treatments for patients.